Renin-Angiotensin-Aldosterone System (RAAS)
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Article at a Glance
- The renin-angiotensin-aldosterone system (RAAS) helps the body maintain blood pressure and fluid balance.
- Generally, the RAAS response is desirable in hypovolemic patients and undesirable in patients with congestive heart failure.
- Clinicians will learn about the pathophysiology of RAAS and different drugs that work on the RAAS system.
The RAAS is a hormone system that regulates blood pressure and fluid balance. When the body has low blood volume or is hypotensive, the kidneys sense they’re not being perfused and release renin into the bloodstream, setting off a chain reaction that results in the release of angiotensin. The renin-angiotensin-aldosterone system (RAAS) regulates blood pressure and fluid balance. Angiotensin I is a hormone that gets converted to angiotensin II, a powerful vasoconstrictor. It elevates blood pressure and improves renal perfusion. Angiotensin II makes the blood vessels “tense” and causes vasoconstriction. Next, aldosterone is released. Aldosterone is the “saltwater hormone.” When aldosterone is released, the body retains sodium and fluid while excreting potassium, increasing blood pressure and perfusing the kidneys. Read: Human Immunodeficiency Virus (HIV)Introduction to the Renin-Angiotensin-Aldosterone System
Related Video – Renin Angiotensin Aldosterone System (RAAS) Physiology
RAAS may adversely affect cardiac patients with congestive heart failure (CHF). Their heart isn’t pumping efficiently, or it’s lost some of its contractility. The kidneys aren’t adequately perfused, so they activate the RAAS system. Activation of the renin-angiotensin-aldosterone system can worsen heart failure. The active RAAS system causes vasoconstriction and retention of sodium and water, which is bad for CHF patients. They don’t need more fluids. Providers should administer angiotensin-converting enzyme inhibitors and ACE inhibitors to counter the reaction. They include the “-pril” drugs, such as lisinopril. ACE-inhibitors block the angiotensin-converting enzyme and stop end reactions. Providers will see reduced vasoconstriction and sodium and increased fluid retention. Vasodilation will present, indicating the body now retains potassium instead of excreting it. Lisinopril is an ACE-inhibitor. ACE-inhibitors block the renin-angiotensin-aldosterone system. Angiotensin receptor blockers (ARBs) are similar to ACE inhibitors. Along with ACE inhibitors, they carry the risk of hyperkalemia due to the anti-aldosterone effects. Additionally, ACE inhibitors affect the bradykinin in the lungs, causing a dry cough. ARBs don’t affect bradykinin or present a dry cough risk. Physicians also administer beta-blockers to treat RAAS in CHF patients. Beta-blockers improve ejection fractions, slowing the heart rate by blocking the sympathetic nervous system from stimulating the beta-receptors. While the heart rate is slowed, the ventricles have more time to fill, which is advantageous for CHF patients. Providers should not administer beta-blockers to a patient in the acute phase of CHF. They reduce the heart’s contractility. If a patient is already hypotensive and bradycardic, reducing contractility and slowing the heart may worsen their condition. The renin-angiotensin-aldosterone system maintains the body’s blood pressure and fluid balance. It works well for hypovolemic patients needing improved renal perfusion. However, it may adversely affect patients with CHF.RAAS in Congestive Heart Failure
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